Protective effects of phosphatidylcholine against mechanisms of ischemia and reperfusion-induced arrhythmias in isolated guinea pig ventricular tissues.
The effects of exogenous phosphatidylcholine (PC) on some potential mechanisms of ischemia and reperfusion-induced arrhythmias were tested using the superfused right ventricular free wall of the guinea pig. Exposure of the preparation to simulated "ischemia" (hypoxia, acidosis, glucose deprivation and hyperkalemia) resulted in several electrophysiological derangements, including a marked depolarization of the maximum diastolic potential (MDP) in both endocardium and epicardium, shortening of the action potential duration (APD), and prolongation of the transmural conduction time followed by transmural conduction block. In a few preparations, coupled beats were also observed. Reperfusion was associated with arrhythmic activity in all preparations. Both the characteristics and the severity of reperfusion-associated arrhythmias were dependent upon the duration of the preceding "ischemia". In hearts exposed to ischemic conditions for 40 min, transmural conduction block persisted until 45 min of reperfusion and no electrical activity was present in the epicardium during this time. However, both coupled beats as well as abnormal automaticity were observed in the endocardium. When the period of "ischemia" was reduced to 20 min, recovery from transmural conduction block occurred sooner and coupled beats and abnormal automaticity were detected in both epicardial and endocardial layers. Superfusion with PC during both "ischemia" and reperfusion (PC1 group), or during reperfusion only (PC2 group), significantly altered the response of the preparations to reperfusion. Following 40 min "ischemia", preparations treated with PC recovered from transmural conduction block more rapidly (PC1 group, 4 min, P less than 0.05; PC2 group, 23 min, ns), compared to control.(ABSTRACT TRUNCATED AT 250 WORDS)
Duan
J M
JM
Department of Pharmacology and Toxicology, University of Western Ontario, London, Canada.
Moffat
M P
MP
D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D000889:Anti-Arrhythmia Agents; D001145:Arrhythmias, Cardiac / Q000209:etiology / Q000503:physiopathology* / Q000517:prevention & control; D003327:Coronary Disease / Q000150:complications / Q000503:physiopathology; D004558:Electric Stimulation; D006168:Guinea Pigs; D006321:Heart / Q000187:drug effects* / Q000502:physiology; D066298:In Vitro Techniques; D008297:Male; D015425:Myocardial Reperfusion; D010713:Phosphatidylcholines / Q000494:pharmacology*
D000889:Anti-Arrhythmia Agents; D010713:Phosphatidylcholines